Heavy drinking is the third leading cause of preventable death in the United States, the second most important cause of disability among adults aged 24-44, and alcohol related problems cost the US an estimated $224 billion each year. Despite the prevalence and individual and societal impacts of AUD, the mechanisms underlying this disorder are not well understood. The aims of this grant are to use a cognitive neuroscience approach to identify the mechanisms that maintain problem drinking (PD) (Aim 1) and to examine how these mechanisms are altered by treatment (Aim 2). A dominant hypothesis is that AUD is characterized by a combination of heightened incentive sensitization to alcohol cues (i.e., cue reactivity) and an impaired ability to regulate cue-induced craving. Heightened reactivity in the brain would be evident by increased reward system activity, particularly in the ventral striatum, whereas impaired regulation would manifest as weak engagement of prefrontal control systems needed to revalue alcohol cues and dampen craving. Unfortunately, scant research exists examining the neural systems underlying cue reactivity in moderate AUD samples, and no study has tested the systems involved in active regulation of cue-induced craving. Therefore, the incentive sensitization hypothesis has not been sufficiently tested, and it is unclear which neural systems support cue reactivity and cognitive regulation of craving in PDs. This gap in knowledge hinders our ability to understand individual differences in the nature and severity of the disorder, to predict responses to treatment, and to understand the mechanism by which treatment changes behavior. The neural and behavioral mechanisms that maintain PD should be impacted by treatment. To probe these mechanisms, we will assess cue reactivity, regulation of cue-induced craving, and drinking in problem drinkers (PDs) at baseline and after 8 weeks of a widfromely disseminated and validated psychosocial intervention for reducing drinking in AUD, Motivational Interviewing (MI). Participants will complete an alcohol cue reactivity and regulation paradigm while undergoing an fMRI scan once at baseline and again after receiving MI treatment or a period of self-change (control condition). We will assess the mechanisms of PD by analyzing the behavioral and neural indices of cue reactivity and regulation to alcohol cues versus other appetitive cues (food) at baseline. We will assess the mechanisms of MI treatment by examining changes in cue reactivity and regulation in the MI group from baseline to post-treatment, relative to the control group. We expect that at baseline, for alcohol cues relative to food cues, PDs will show heightened craving and reward system activation, impaired ability to reduce craving using regulation strategies, and weaker recruitment of prefrontal control regions during regulation (Aim 1). We predict that MI will a) reduce craving and decrease reward system activity during natural responding and b) bolster regulation success and increase engagement of the prefrontal cortex during regulation (Aim 2).